NFS1 antibody - middle region (ARP33115_T100)
- Known as:
- NFS1 (anti-) - middle region (ARP33115_T100)
- Catalog number:
- arp33115_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NFS1 antibody - middle region (ARP33115_T100)
Related genes to: NFS1 antibody - middle region (ARP33115_T100)
- Gene:
- NFS1 NIH gene
- Name:
- NFS1 cysteine desulfurase
- Previous symbol:
- -
- Synonyms:
- NifS, IscS
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-01
- Date modifiied:
- 2019-01-21
Related products to: NFS1 antibody - middle region (ARP33115_T100)
Related articles to: NFS1 antibody - middle region (ARP33115_T100)
- NFS1 (cysteine desulfurase), an essential enzyme in iron-sulfur (FeS) cluster biogenesis, is a key regulator of ferroptosis. In oral squamous cell carcinoma (OSCC), NFS1 is up-regulated and undergoes enhanced succinylation under glucose starvation. This study aims to elucidate the mechanistic role of NFS1, particularly through ferroptosis, in OSCC progression. - Source: PubMed
Publication date: 2026/04/23
Ling HangQing LiminZuo LiangWang HonghanCai XuLiu YanTian Hao - Delineating how acquired nutrients are partitioned into different intracellular pathways and how these various fates support distinct functions in T cells is limited. We show that CD8 T cells acquire cysteine to serve both as a substrate for glutathione (GSH) production, which modulates effector functions, and to cede its sulfur for NFS1-dependent FeS cluster synthesis, which supports proliferation. NFS1 deletion in activated CD8 T cells promotes exhaustion and dampens anti-cancer immunity, whereas blocking cysteine flux into GSH or enforcing FeS metabolism enhances tumor control. This role for disrupted FeS metabolism in T cell exhaustion is echoed in data from human hepatocellular carcinoma. Elucidating how different intracellular pathways use cysteine enables targeted control of cysteine flux to retain the beneficial effects of cysteine while abolishing those that restrain function. We illustrate this concept for one metabolite, cysteine, but it is likely to apply to other metabolites relevant for immune cell function. - Source: PubMed
Publication date: 2026/03/31
Kelly BethCha MinsunGremelspacher TatjanaMartin Jacob LAndreis MassimoMaloo IshaCarrizo Gustavo EGidley MiaStanczak Michal AApostolova PetyaLongo JosephDeCamp Lisa MMa Eric HSheldon Ryan DJones Russell GSanin David EMajumdar AnanyaPearce Erika L - Fish are ectothermic animals that are highly sensitive to water temperature fluctuations, and elevated temperatures can readily trigger stress responses. Gills, the primary organ for respiration and osmoregulation in fish, are directly exposed to the water environment and therefore highly susceptible to high-temperature (HT) stress. In this study, the juvenile Trachinotus ovatus were exposed to acute HT stress for 7 days, then the histological morphology, oxidative stress, ferroptosis, and metabolite profiling were systematically investigated. The results showed that HT stress caused pronounced structural damage to the gill tissues, and induced oxidative stress by increasing the hydrogen peroxide content and enhancing CAT and GPx activities, whereas decreasing SOD activity. Antioxidant signaling, including Nrf2, Keap1, and HO-1 genes expression were increased, while NQO1 gene expression was decreased. In addition, the ferroptosis homeostasis was disrupted, characterized by increased iron content and upregulated expression of NOXA1, NCOA4 and PTGS2 genes, as well as decreased Cys levels and downregulated expression of SLC7A11, GPx4, p53, FTH1, and NFS1 genes. Furthermore, the metabolic profile was also affected, particularly the functions of ATP-binding cassette (ABC) transporters, tricarboxylic acid cycle, and multiple amino acid metabolism. Alterations in several functional metabolites, such as L-tyrosine, fumaric acid, and 2,3-dinor-8-iso-prostaglandin F2α, were involved in antioxidant defense, energy metabolism, and iron homeostasis. Collectively, these findings indicated that acute HT stress affected the histomorphology, redox status, ferroptosis homeostasis, and metabolite profiles in the gills of T. ovatus, which might interfere with its physiological functions. - Source: PubMed
Publication date: 2026/03/30
Zhu RuijieXiao MengHuang XiaohuaZhang DianchangZhou FalinGuo HuayangYang YukaiDuan Yafei - Ferroptosis is emerging as a crucial type of cellular demise involved in intracerebral hemorrhage (ICH). Cysteine desulfurase (NFS1) is a key gene involved in the regulation of ferroptosis; however, its role in modulating neuronal ferroptosis in ICH remains unclear. This work aimed to explore whether NFS1 influences neuronal ferroptosis in ICH and to explore the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/02/17
Wang XiaohuFeng YanweiMa Jiuhong - Delineating how acquired nutrients are partitioned into different intracellular pathways, and how these various fates support distinct functions in T cells is limited. We show that CD8 T cells acquire cysteine to serve both as a substrate for glutathione (GSH) production, which modulates effector functions, and to cede its sulfur for NFS1-dependent FeS-cluster synthesis, which supports proliferation. NFS1 deletion in activated CD8 T cells promotes exhaustion and dampens anti-cancer immunity, while blocking cysteine flux into GSH, or enforcing FeS metabolism, enhance tumor control. This role for disrupted FeS metabolism in T cell exhaustion is echoed in data from human HCC. Elucidating how different intracellular pathways use cysteine enables targeted control of cysteine flux to retain beneficial effects of cysteine while abolishing those that restrain function. We illustrate this concept for one metabolite, cysteine, but it is likely to apply to other metabolites relevant for immune cell function. - Source: PubMed
Publication date: 2026/01/29
Kelly BethCha MinsunGremelspacher TatjanaMartin Jacob LAndreis MassimoCarrizo Gustavo EGidley MiaStanczak Michal AApostolova PetyaSanin David EMajumdar AnanyaPearce Erika L